Effect of acetazolamide administration on some hematological parameters of rainbow trout: 24 hrs after administration there was no effect on the oxygen dissociation curve for whole blood but RBC volume was significantly increased and the amount of oxygen carried per gm. hemoglobin was decreaded. The Root effect occurred even at PO2 of 450 torr and in the absence of functional carbonic anhydrase (CA). The rapid depletion of PO2 in the trout eyes following acetazolamide treatment is apparently not due to a decrease in the supply of oxygen to the counter current multiplier via the blood. Importance of counter current oxygen multiplier mechanism in maintaining retinal function in the teleost: Within minutes of admin. of acetazolamide changes in the electroretinogram (ERG) occurred which were subsequently associated with retrieval hypoxia. In vitro inhibition of CA with acetozalomide in the frog and trout retina produced no changes in the ERG thus the drug had no direct effect on the retina. In vitro studies also indicated that trout ERG's could not be maintained at arterial PO2 levels indicating the vascular trout retina. Oxygen toxicity in retina, brain and liver tissue of the trout, frog and dog: Trout retinal metabolism was not inhibited after 24 hrs exposure to hyperbaric (1470 torr) oxygen but dog retinal tissue showed a significant decrease in carbohydrate metabolism with similar treatment. Elevated oxygen tensions caused deleterious metabolic effects in hepatic and brain tissue of all three species and the higher the metabolic rate of a tissue the more susceptible it was to oxygen toxicity. Decreasing temperature caused a lowered susceptability to oxygen toxicity.